Can you please tell viva questions along with answer from hematology
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I now have rich content from the textbooks. Let me compile a comprehensive viva Q&A for MBBS undergraduates across all hematology topics.
Hematology Viva Questions & Answers (MBBS Undergraduate)
SECTION 1: Anemias - Iron Deficiency Anemia
Q1. What is the most common nutritional deficiency worldwide?
Iron deficiency. It is the most common nutritional deficiency in the world and the most frequent cause of anemia. It affects ~10% of people in high-resource countries and 25-50% in lower-resource countries.
(Robbins & Kumar Basic Pathology)
Q2. What is the normal total body iron content? How is it distributed?
- Total body iron: ~2.5 g in women, ~3.5 g in men
- ~80% is "functional iron" - found in hemoglobin, myoglobin, and iron-containing enzymes (catalase, cytochromes)
- ~15-20% is in the "storage pool" as hemosiderin and ferritin, mainly in macrophages of liver, spleen, and bone marrow
Q3. How is dietary iron absorbed?
Absorption occurs in the duodenum:
- Ferric iron (Fe3+) is reduced to ferrous iron (Fe2+) by duodenal cytochrome B (ferric reductase)
- Fe2+ crosses the apical membrane via DMT-1 (divalent metal transporter-1)
- Fe2+ crosses the basolateral membrane into plasma via ferroportin
- In plasma, iron is oxidized back to Fe3+ by hephaestin/ceruloplasmin and binds to transferrin
Q4. What is hepcidin? What is its role?
Hepcidin is a small peptide secreted by the liver. It negatively regulates ferroportin, thus blocking iron export from enterocytes and macrophages into plasma. When iron stores rise, HFE protein on hepatocytes senses this and upregulates hepcidin, reducing absorption (negative feedback loop). Inflammatory mediators (IL-6) also increase hepcidin - this is why anemia of chronic disease occurs.
Q5. What are the stages of iron deficiency?
- Pre-latent stage - Depletion of iron stores; serum ferritin falls; no anemia yet
- Latent (iron-deficient erythropoiesis) - Serum iron falls, TIBC rises, transferrin saturation falls; still no anemia
- Iron deficiency anemia - Hemoglobin falls; microcytic hypochromic anemia appears
Q6. What are the typical lab findings in iron deficiency anemia?
| Parameter | Finding |
|---|---|
| Serum iron | Decreased |
| Serum ferritin | Decreased (best early marker) |
| TIBC (transferrin) | Increased |
| Transferrin saturation | Decreased (<16%) |
| Blood film | Microcytic, hypochromic RBCs; pencil cells (elliptocytes) |
| RDW | Increased (anisocytosis) |
| Reticulocyte count | Low |
Q7. What are clinical features specific to iron deficiency (beyond anemia)?
- Koilonychia (spoon-shaped nails)
- Glossitis, angular stomatitis (atrophic tongue)
- Pica (craving for non-food substances like clay or ice - "pagophagia")
- Plummer-Vinson syndrome (postcricoid dysphagia + iron deficiency anemia + esophageal web)
- Blue sclerae
SECTION 2: Megaloblastic Anemia
Q8. What is the pathophysiology of megaloblastic anemia?
Vitamin B12 and folic acid are cofactors required for synthesis of thymidine (one of the four DNA bases). Deficiency results in defective nuclear maturation due to impaired DNA synthesis, with a block in cell division. Cytoplasm continues to grow while the nucleus lags - producing large cells ("megaloblasts"). This leads to ineffective hematopoiesis (cells die in the marrow before release).
(Robbins, Cotran & Kumar Pathologic Basis of Disease)
Q9. What are the causes of Vitamin B12 deficiency?
- Decreased intake: Strict vegetarianism (B12 only in animal products)
- Impaired absorption:
- Intrinsic factor (IF) deficiency - Pernicious anemia (autoimmune destruction of parietal cells), gastrectomy
- Ileal resection or ileitis (terminal ileum is site of B12-IF complex absorption)
- Diffuse intestinal disease (lymphoma, systemic sclerosis)
- Competitive uptake: Fish tapeworm (Diphyllobothrium latum), bacterial overgrowth
Q10. What is Pernicious anemia?
An autoimmune condition where antibodies destroy gastric parietal cells or block intrinsic factor. Parietal cells produce both HCl and intrinsic factor (IF). Without IF, B12 cannot be absorbed in the terminal ileum. Associated with type A chronic gastritis (fundus/body). Anti-parietal cell antibodies and anti-IF antibodies are found.
Q11. What are the causes of folate deficiency?
- Decreased intake: Poor diet, alcoholism, infancy
- Impaired absorption: Malabsorption states; drugs (anticonvulsants, oral contraceptives)
- Increased requirement: Pregnancy, infancy, disseminated cancer, hemolysis
- Increased loss: Hemodialysis
- Impaired utilization: Folic acid antagonists (methotrexate)
Q12. How do you differentiate B12 from folate deficiency on peripheral smear?
Both show identical peripheral smear changes - macrocytes, macro-ovalocytes, and hypersegmented neutrophils (>5 lobes in a neutrophil, or any neutrophil with 6+ lobes). Lab values (serum B12, serum folate, RBC folate, methylmalonic acid, homocysteine) are needed to differentiate.
Q13. What are the neurological features unique to B12 deficiency (not folate)?
Subacute combined degeneration (SCD) of spinal cord - demyelination of:
- Posterior columns (loss of vibration sense, proprioception)
- Lateral (corticospinal) tracts (spasticity, hyperreflexia)
Also: peripheral neuropathy, optic atrophy, dementia. Folate does NOT cause neurological damage.
SECTION 3: Hemolytic Anemias
Q14. How do you classify hemolytic anemias?
By mechanism:
- Intrinsic (intracorpuscular) - defects within the RBC itself (usually hereditary): membrane defects (hereditary spherocytosis), enzyme defects (G6PD deficiency, pyruvate kinase deficiency), hemoglobin defects (sickle cell, thalassemia)
- Extrinsic (extracorpuscular) - factors outside the RBC (usually acquired): autoimmune, microangiopathic (TTP, HUS, DIC), malaria, hypersplenism
By site of destruction:
- Intravascular hemolysis: Within blood vessels - hemoglobinuria, hemoglobinemia, reduced haptoglobin. Causes: G6PD deficiency, ABO incompatibility, PNH, MAHA
- Extravascular hemolysis: RBCs destroyed by macrophages in liver/spleen - jaundice, splenomegaly. Causes: hereditary spherocytosis, autoimmune hemolytic anemia
Q15. What are the general lab features of hemolytic anemia?
- Anemia (normocytic usually)
- Elevated bilirubin (unconjugated/indirect) - jaundice
- Elevated LDH
- Reduced haptoglobin (haptoglobin binds free hemoglobin released from lysed RBCs)
- Elevated reticulocyte count (bone marrow compensation)
- Hemoglobinuria/hemosiderinuria in intravascular hemolysis
Q16. What is Hereditary Spherocytosis?
Autosomal dominant (mostly) defect in RBC membrane skeleton proteins, most commonly spectrin or ankyrin. Loss of membrane leads to spherical (non-biconcave) RBCs with reduced surface area:volume ratio. Spherocytes are rigid and destroyed by splenic macrophages.
- Peripheral smear: spherocytes (lack central pallor), polychromasia
- Osmotic fragility test: increased (spherocytes lyse at lower salt concentrations)
- AGLT (Acidified Glycerol Lysis Test): used as a screening test
- Treatment: splenectomy
Q17. What is G6PD deficiency? Why do patients present with episodic hemolysis?
G6PD (Glucose-6-phosphate dehydrogenase) is an enzyme in the pentose phosphate pathway. It produces NADPH, which is needed to regenerate glutathione (protects RBCs from oxidative damage). In G6PD deficiency, oxidative stress (from infections, certain drugs - primaquine, dapsone, sulfonamides, or foods like fava beans) causes denaturation of hemoglobin forming Heinz bodies, which are pitted by the spleen, creating "bite cells" on smear. Episodes are self-limiting because older RBCs (lowest G6PD) are destroyed first; newer reticulocytes have enough G6PD to survive.
SECTION 4: Leukemias and Lymphomas
Q18. How do you classify leukemia?
| Acute | Chronic | |
|---|---|---|
| Myeloid | AML (Acute Myeloid Leukemia) | CML (Chronic Myeloid Leukemia) |
| Lymphoid | ALL (Acute Lymphoblastic Leukemia) | CLL (Chronic Lymphocytic Leukemia) |
- Acute leukemias: proliferation of blasts (>20% blasts in bone marrow by WHO criteria)
- Chronic leukemias: proliferation of more mature cells
Q19. What is the Philadelphia chromosome? What leukemia is it associated with?
The Philadelphia (Ph) chromosome is a translocation t(9;22)(q34;q11). It results in the fusion gene BCR-ABL on chromosome 22. BCR-ABL encodes a constitutively active tyrosine kinase, driving uncontrolled proliferation. It is present in:
- CML (>95% of cases) - the hallmark
- Some cases of ALL (~25% of adult ALL, ~5% of childhood ALL)
Q20. What are the clinical features of CML?
- Insidious onset, middle-aged adults
- Massive splenomegaly (most common finding)
- Leukocytosis (WBC often >100,000/µL)
- All stages of myeloid maturation seen on smear ("left shift") - myelocytes, metamyelocytes, bands
- Basophilia (characteristic)
- Low leukocyte alkaline phosphatase (LAP) score (distinguishes from leukemoid reaction, which has high LAP)
- Three phases: Chronic → Accelerated → Blast crisis (transformation to AML or ALL)
- Treatment: Imatinib (tyrosine kinase inhibitor targeting BCR-ABL)
Q21. What is ALL? Who does it affect most?
Acute Lymphoblastic Leukemia - neoplastic proliferation of lymphoblasts (B or T cell precursors). Most common malignancy of childhood (peak 2-5 years). Also occurs in adults (worse prognosis in adults). B-ALL is more common than T-ALL. Presents with: anemia, thrombocytopenia, bone pain, lymphadenopathy, hepatosplenomegaly, CNS involvement (meningeal spread).
Q22. What markers are used to diagnose ALL vs AML?
- ALL: TdT (terminal deoxynucleotidyl transferase) positive; CD10 (CALLA), CD19, CD20 (B-cell markers); CD3, CD7 (T-cell markers)
- AML: Myeloperoxidase (MPO) positive; Auer rods on smear (pathognomonic); CD13, CD33, CD34; Sudan black B stain positive
Q23. What is the difference between Hodgkin lymphoma (HL) and Non-Hodgkin lymphoma (NHL)?
| Feature | Hodgkin Lymphoma | Non-Hodgkin Lymphoma |
|---|---|---|
| Hallmark cell | Reed-Sternberg cell (RS cell) | No RS cell |
| Spread | Contiguous, predictable | Non-contiguous, unpredictable |
| Extranodal | Rare | Common |
| B symptoms | Common | Variable |
| Peak age | Bimodal (15-35 & >55) | Older adults |
| Prognosis | Generally better | Variable |
Q24. What is a Reed-Sternberg cell?
A large cell with bilobed nucleus (or two separate nuclei) each containing a prominent "owl-eye" nucleolus, and abundant cytoplasm. It is the hallmark of Hodgkin lymphoma. RS cells are neoplastic B cells (CD15+, CD30+). Classic RS cell must be present for diagnosis; "variants" include lacunar cells (nodular sclerosis subtype) and lymphocytic/histiocytic (L&H/"popcorn") cells.
SECTION 5: Bleeding Disorders and Coagulation
Q25. How do you classify bleeding disorders?
- Vascular defects: Henoch-Schönlein purpura, scurvy, hereditary hemorrhagic telangiectasia
- Platelet disorders:
- Thrombocytopenia (reduced count): ITP, TTP, HUS, drug-induced
- Platelet dysfunction (normal count): von Willebrand disease, Glanzmann thrombasthenia, Bernard-Soulier
- Coagulation factor deficiencies:
- Intrinsic pathway: Hemophilia A (Factor VIII), Hemophilia B (Factor IX)
- Extrinsic/common pathway: Factor VII, X, V, II deficiencies; liver disease; DIC
Q26. How does the pattern of bleeding differ between platelet disorders and coagulation disorders?
| Feature | Platelet/Vascular Defect | Coagulation Factor Defect |
|---|---|---|
| Bleed type | Mucosal, skin | Deep tissue, joints |
| Petechiae/purpura | Present | Absent |
| Hemarthrosis | Rare | Classic (Hemophilia) |
| Bleeding after cuts | Immediate, prolonged | Delayed |
| Screening test | BT (bleeding time), platelet count | PT, aPTT |
Q27. What is Hemophilia A? How is it inherited?
Hemophilia A is an X-linked recessive disorder due to deficiency of Factor VIII. Males are affected, females are carriers. Presents with hemarthrosis (joint bleeds), muscle hematomas, easy bruising. Laboratory: elevated aPTT, normal PT, normal bleeding time, reduced Factor VIII activity. Treatment: recombinant Factor VIII concentrate; DDAVP (desmopressin) for mild cases (releases stored vWF-Factor VIII complexes).
Q28. What is von Willebrand disease (vWD)?
The most common inherited bleeding disorder. von Willebrand factor (vWF) is a multimeric protein made by endothelium and megakaryocytes. It has two roles:
- Platelet adhesion at injury site (bridges GPIb on platelets to collagen)
- Carrier protein for Factor VIII in plasma (protects it from degradation)
Most common form (Type 1): autosomal dominant, partial quantitative deficiency. Presents with mucocutaneous bleeding (epistaxis, menorrhagia). Labs: prolonged bleeding time, prolonged aPTT (because Factor VIII is low), normal PT. Treatment: DDAVP, Factor VIII/vWF concentrate.
Q29. What is DIC (Disseminated Intravascular Coagulation)?
DIC is an acquired coagulopathy characterized by widespread activation of the coagulation system, leading to:
- Microvascular thrombosis (occludes small vessels - causes organ failure)
- Consumption of clotting factors and platelets (causes bleeding)
Causes: Sepsis (most common), obstetric emergencies (amniotic fluid embolism, abruptio placentae), trauma, malignancy, snake venom, transfusion reactions.
Lab findings: Prolonged PT + aPTT, low fibrinogen, low platelets, elevated D-dimers/FDP, schistocytes (microangiopathic hemolysis) on smear.
SECTION 6: Blood Groups and Transfusion
Q30. What are the ABO blood groups? Who discovered them?
Discovered by Karl Landsteiner in 1900. The ABO system is based on antigens on the RBC surface and corresponding antibodies in plasma:
| Blood Group | RBC Antigen | Plasma Antibody | Universal |
|---|---|---|---|
| A | A | Anti-B | - |
| B | B | Anti-A | - |
| AB | A and B | None | Universal recipient |
| O | None | Anti-A and Anti-B | Universal donor |
ABO antibodies are naturally occurring IgM (no prior sensitization needed).
Q31. What is the Rh blood group system?
The Rh system is the second most clinically important blood group system. The most important antigen is Rh D antigen. Rh-positive (D antigen present) vs Rh-negative (D antigen absent). Unlike ABO, Rh antibodies are NOT naturally occurring - anti-D develops only after exposure to Rh+ blood (via transfusion or pregnancy).
Q32. What is Hemolytic Disease of the Newborn (HDN / Erythroblastosis Fetalis)?
Occurs when an Rh-negative mother carries an Rh-positive fetus (inherited from Rh+ father). During first pregnancy, fetal RBCs cross the placenta at delivery, sensitizing the mother to produce IgG anti-D antibodies. In a subsequent Rh+ pregnancy, maternal IgG anti-D crosses the placenta (IgG crosses placenta, IgM does not), destroys fetal RBCs, causing hemolytic anemia, jaundice, and hydrops fetalis.
Prevention: Rh immunoglobulin (RhoGAM/anti-D) given to Rh- mothers at 28 weeks and within 72 hours of delivery/miscarriage/sensitizing event. It destroys fetal RBCs in maternal circulation before sensitization can occur.
Q33. What are the indications and types of blood products for transfusion?
| Product | Contents | Indication |
|---|---|---|
| Packed RBCs | RBCs | Anemia, acute blood loss |
| Platelets | Platelets | Thrombocytopenia (<10,000 or bleeding) |
| Fresh Frozen Plasma (FFP) | All clotting factors | DIC, warfarin reversal, liver disease |
| Cryoprecipitate | Factor VIII, vWF, fibrinogen, Factor XIII | Hemophilia A, vWD, DIC (low fibrinogen) |
| Whole blood | Everything | Massive hemorrhage |
Q34. What are the complications of blood transfusion?
Immunological:
- Acute hemolytic transfusion reaction (ABO incompatibility) - most dangerous; fever, chills, hemoglobinuria, renal failure, DIC. Caused by preformed IgM antibodies (intravascular hemolysis)
- Delayed hemolytic reaction (Rh or other minor antigen incompatibility) - occurs 3-10 days later (IgG, extravascular)
- Febrile non-hemolytic reaction (most common overall) - antibodies to donor leukocyte antigens
- Allergic reactions (to plasma proteins)
- Transfusion-Related Acute Lung Injury (TRALI) - non-cardiogenic pulmonary edema within 6 hours
- Graft vs Host Disease (immunocompromised recipients)
Non-immunological:
- Infections (HIV, Hepatitis B/C)
- Iron overload (multiple transfusions - hemosiderosis)
- Hypothermia, hypocalcemia (from citrate in stored blood), hyperkalemia
QUICK REFERENCE: Key Mnemonics for Viva
- Causes of microcytic anemia - "TAILS": Thalassemia, Anemia of chronic disease, Iron deficiency, Lead poisoning, Sideroblastic anemia
- Causes of macrocytic anemia - "B12/Folate, Liver disease, Hypothyroidism, Alcohol, Reticulocytosis, Drugs (hydroxyurea)"
- DIC lab findings - "All tests prolonged + Platelets down + Fibrinogen down + D-dimers up"
- Reed-Sternberg cell - "Owl-eye" appearance; CD15+ and CD30+
- Hemophilia A vs B - A = Factor VIII ("A-te"), B = Factor IX ("B-nine")
- ABO antibodies are IgM (naturally occurring, don't cross placenta); Rh antibodies are IgG (immune, cross placenta)
Sources: Robbins & Kumar Basic Pathology; Robbins, Cotran & Kumar Pathologic Basis of Disease; Goldman-Cecil Medicine; Henry's Clinical Diagnosis & Management by Laboratory Methods; Emery's Elements of Medical Genetics and Genomics
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